An Atlas of Bovine

Diseases and Syndromes

Dr. Ted Clark

Animal CARE Centre
Animal Diagnostic Laboratory
Calgary, Alberta
Canada
clark@carecentre.ca
VIRAL DISEASES
 BVDV - Bovine Virus Diarrhea
Virus
• genus pestivirus, family Flaviviridae
• Other members: Hog Cholera and Border Disease
virus
• The diversity of BVDV
1) Serotype - one serotype
2) Biotypes - NCP (noncytopathic / wild) and CP
(cytopathic /mutant)
3) Genotype - “type”
type I and II
4) Antigenicity - many strains; pathogenicity
differences, tissue tropism differences
• MLV vaccines
i are CP virus;
i vaccine
i pressure liklikely
l
creating new strains
 BVDV - associated diseases &
syndromes
• 1) Subclinical
S b li i l BVD
• 2) Acute/chronic mucosal disease (MD) (PI cattle)
• 3) Peracute BVD/MD (Ont, Que, NE-US)NE US)
• 4) Thrombocytopenia with hemorrhagic diathesis
• 5) Reproductive failure -embryonic death, abortions,
stillbirths neonate nonviable fetuses
stillbirths,
• 6) Congenital defects
• 7)) Primaryy p
post-natal infection & co-associated
infections, e.g. CPPS with Mycoplasma bovis, or
other infectious agents with more extensive lesions
* Persistently infected (PI) *Not
Not PI
2,5 above 1,3,4,5,6,7 above
 BVDV - cont’d
• In our experience
p with almost 20 yyears of having
g IHC available for use on formalin fixed
tissues, transient (‘acute’, ‘primary’) BVDV infections in the feedlot, with or without
secondary infections, is far more common than persistently infected (PI) cases, with or
without mucosal disease. The PI animal however, is undoubtedly the source of infection
for the primary BVD cases.
cases
• We have been fortunate to NOT having experienced the acute primary BVDV infections
experienced in Ontario And Quebec in the early 90s. Grossly and histologically, these
pp
apparently y cannot be distinguished
g from PI animals with mucosal disease.
• A hallmark feature of primary BVDV histologically is varying degrees of arteritis or
proliferative arteriopathy in heart, lung,and sometimes other tissues and these are often
the only sites where IHC for viral antigens is positive. We do not see arteritis in PI
animals except rarely. Viral lymphocytic and necrotizing myocarditis is also common in
these cases if it is looked for. Gross lesions give you no clue to this syndrome, unless
there are obvious CPPS lesions, with Mycoplasma bovis in lung and/or joints.
• In addition to,
to or instead of CPPS,
CPPS unusually extensive lesions of many commonly
occurring bacterial and viral infections in feedlots should be considered to be
predisposed to by primary BVDV infections, as a result of severe immunosuppression.
For e.g., severe mannheimiosis later in the feeding period than expected, or extensive
papular stomatitis or IBR lesions should be suspected of co-existing primary BVDV
infection. Do not expect to find gross lesions of BVDV in these cases. Multiple sections
of heart, lung and ileum are still the best tissues to examine in these cases.
 BVDV lesions of the GIT
• Typically the persistently infected/PI animal that dies of mucosal disease has
necrosis/ulceration/hemorrhage over Peyer’s patches plus lesions in other sites e.g.
oral cavity and esophagus.
• Not all feedlot cattle that are PI however die of mucosal disease-
disease these cases may have
much milder to no typical MD lesions and die of other infectious diseases such as
mannheimiosis, hemophilosis or even coccidiosis.
• Best
est way now
ow to confirm
co or
o rule
u e out a PI animal
a a iss submit
sub t a ppiece
ece of
o sskin from
o
anywhere on the body for IHC for BVDV. Submit these in formalin only. Another
type of mucosal disease is called chronic mucosal disease and these will often show
only mild esophageal and oral lesions if any at all and often chronic intestinal lesions
only.
l The
Th PP important
i t t to
t examine
i grossly l carefully
f ll in
i these
th cases. These
Th will
ill still
till be
b
positive for PI on skin IHC.
• Primary BVD lesions in the intestinal tract are usually only severe atrophy of PP, a
histo diagnosis only, or die of some other secondary bacterial, or fungal infections.
Most primary BVDV cases are lung viral or bacterial infections with no intestinal
lesions. These are secondary infections due to immunosuppression.
• Areas of depigmentation of ruminal or omasal mucosa is often due to chronic BVDV
in PI individuals. Abomasal ulcers also occur in some PI cattle, but not all abomasal
ulcers are due to BVDV.
Transient BVD – IHC study 277
consecutive post mortems
Proportion of BVD IHC Positive Results
by Tissue Location
30.0%

25.0%

20.0%

15.0%

10.0%

5.0%

0.0%
Heart Lung Ileum Skin

Dr. John Campbell, unpublished material

 Enteric coronavirus

• One of the most important causes of neonatal calf

diarrhea in western Canada
•Especially important because of high death loss and lack
of response to therapy
•Negative electron microscopy of feces to diagnose but
IHC works well, especially on spiral colon sections
•Histo lesions characteristic and colon best if dead several
hours
•Severe cryptitis
yp with loss of villus epithelium
p is a
hallmark feature
•Severe atrophy/depletion of Peyer’s patches and thymus
•Small miliary abomasal ulcers common but not
pathognomonic for
 BRSV – bovine respiratory syncytial virus
infection
• We see this
W thi muchh more commonly l in
i cow-calflf operations
ti than
th feedlot
f dl t calves.
l
• Occurs in two forms and are considered stages or phases of the disease. Seldom do calves with phase I develop
phase II disease and most phase I cases recover completely or are subclinical
• Phase I is a syncytial cell bronchiolitis and most cases recover and some are not clinical. The morbidity rate is
high but mortality low
low.Very
Very high fevers is typical clinically
clinically.
• Phase II often occurs up to a month later and calves die suddenly or after a few hours of severe respiratory
distress with an expiratory grunt. The incidence of this is low.
• Phase I lesions are mainly cranial ventral, dark firm lung tissue with varying amounts of subpleural, bullous and
interlobular emphysema. Histopathology can easily make this diagnosis and IHC or DIF easily can identify virus
in airways and alveoli. Multiple sections of lung from various sites are important. Only one lung or the other
needs to be sampled. Extension into caudal lung lobes common in fatal cases.
• Phase II lesions are essentially the same as feedlot interstitial pneumonia and areas of subpleural emphysema are
the best areas in which to still find syncytial cells to allow the pathologist to confirm the diagnosis. Often
however, no BRSV antigens found so certainly most feedlot AIP lungs cannot be confirmed as due to BRSV.
Cranial lung lobes are the best to find BRSV antigens in such cases.
• The mechanism of interstitial pneumonia due to this virus is unknown but experimentally a combination of 3
methyl indole and BRSV causes more severe pneumonia than BRSV alone. However, the typical feedlot AIP
lung has still not been experimentally reproduced to my knowledge.
knowledge
• BRSV often results in a ‘bronchiolar’ pattern in the lungs, and this is often due to bronchiolitis obliterans.
IBR/BHV1 – Infectious Bovine Rhinotracheitis
• Most common manifestation of is typical upper respiratory tract disease with rhinitis,
conjunctivitis If death occurs,
conjunctivitis. occurs postmortem typically reveals fibrinous and necrotizing
tracheitis, bronchitis, bronchiolitis and laryngitis.
• Severe cases and especially concurrently with primary BVDV infection, we will see
focal ulcerative stomatitis, esophagitis and even rumenitis as well. Lesions in the
esophagus and rumen will often be white and raised rather then ulcerative or erosive.
• Typically a necrotizing bronchiolitis with secondary bacterial bronchopneumonia also
is often present and viral inclusion bodies with positive DIF or IHC in the cranial
aspects of the lung is present.
present We have seen outbreaks of pneumonia in beef calves on
pasture and the diagnosis was initially missed because the pneumonia was more severe
and striking than the laryngitis/tracheitis or the connection between the two was not
made.
• Lung involvement needs to be differentiated from necrotizing laryngitis and aspiration
pneumonia from other bacterial causes.
• IHC on formalin fixed tissues is highly specific and accurate on all strains of virus
• Rarely IBR encephalitis seen without upper respiratory tract lesions.
 Rota ir s
Rotavirus
• Another cause of neonatal diarrhea but usually not by
itself fatal
•Predisposes to E. coli or Cryptosporidia sp.
•Milder
Milder, more transient infection than E.E coli or
coronavirus
•No colonic lesions as in coronavirus
•IHC
IHC works k wellll in
i pigs
i but
b t nott calves
l
•Direct immunofluorescence or negative EM studies best
within the first 5 days of infection
•No characteristic gross lesions
•Group A of 5 mammalian pathogenic rotaviruses
 Bovine Papular Stomatitis
• Usually when seen is of no clinical significance except to
consider that the animal is likely immunosuppressed.
immunosuppressed Often
seen in primary or transient BVDV infections
• Lesions most commonlyy on the hard and soft ppalate but if
extensive, can be in the esophagus, on the tongue, on the
muzzle/nostrils and on the gingiva. In the esophagus are
round or oval rather than typical linear BVDV lesions
• Often appears as grayish or erosive circular areas with raised
edges. Gray, outer raised rims common. Histo shows irregular,
granular, basophilic inclusion bodies in squamous epithelial
cell cytoplasm.
• We do not have IHC for any of the pox or parapox infections
 Pseudocowpox virus
• Parapoxvirus
Parapo ir s and common in North America
•Lesions only on teats
•Lesions pass through stages of papules, vesicles,
pustules, scabs then regenerative epidermal hyperplasia
lasting for months
•Slow,
Slow, prolonged passage through herds
•Necrotic stage lesions are umbilicated centrally
•Intracytoplasmic viral inclusion bodies to confirm
•Zoonosis in man called milker
•Zoonosis, milker’ss nodules
 Rabies virus
• Federally reportable disease in all of North America
•Rhabdovirus, incubation period 2 weeks to several months
depending on where the virus enters the body
•Of
O farm
a aanimals,
a s, most
ost often
o te seen
see in cattle
catt e
•Mild/paralytic or furious forms in cattle
•Skunks, foxes, raccoons and bats important in transmission
•Always consider with any obscure neurologic signs
•IHC works extremely well on fixed tissues
•Do not rely on seeing Negri bodies, especially in horses and
pigs
•“the only typical clinical finding is its atypicalness”
 Adenoviruses
• In cattle can be seen associated with respiratory and enteric
i f ti
infections
•Diarrhea can be hemorrhagic
•Intranuclear inclusion bodies seen in tracheal or lung airway
epithelial cells and endothelial cells of vessels most often
•Adult cows are carriers for calves
•Latent
Latent infections can recrudesce
•Possibly a role in enzootic pneumonia of calves
•IHC works well to identify in fixed tissues for all strains in all
species
•Occasional diarrhea cases in feedlot cattle
 PI3 virus pneumonia

• In my opinion,
opinion does not cause significant disease in feedlot cattle
except for some chronic bronchiolitis obliterans lesions which can
then play a role in cranial-ventral collapse and perhaps then
predispose
di tto AIP/i
AIP/interstitial
t titi l pneumonia,i Mycoplasma
M l bovis
b i
infection or bronchiectasis.
• More important in some cases of enzootic pneumonia of dairy
calves.
• Similar syncytial cells of airways as in BRSV but smaller and do
not last
l more than h a few
f days
d
• Most feedlot cattle IHC cases seen in BVDV / PI animals where
antigen amounts in the lung can be high, presumably due to
immunosuppression
 Bovine Herpesvirus 2
• In
I North
N hA America
i causes two di diseases, ulcerative
l i
mammillitis and pseudolumpy skin disease
•The latter results in skin edema, necrotic lesions in multiple
p
animals on all parts of the body, usually in adult cows
•Histologically epidermal and follicular epithelial necrosis
with syncytial cells and numerous distinct intranuclear
inclusion bodies
•Virus easy to culture in tissue cultures
 Malignant catarrhal fever

• two forms, alcelaphine in wild ruminants including

game farm animals and ovine herpesvirus 2 in cattle,
bison and deer ((‘sheep
sheep-associated
associated’))
•Classic lesion in cattle is a necrotizing vasculitis in
multiple organs and tissues and nonsuppurative
encephalitis
•In the skin also see single cell necrosis of follicular and
epidermal
p epithelial
p cells,, similar to BVDV infection
•No IHC available to identify, polymerase chain
reaction/PCR tests the best
 P ill
Papillomaviruses
i

• Papovaviridae family of viruses

•Five+ strains in cattle so far, types 1, 5 and 6 cause warts
(verrucae) on haired skin
•Three strains reported specifically on teats
•IHC reagent works on all strains and works nicely on
fixed tissues
•Lesions in the esophagus and rumen as well
•Lice and flies mayy aid in spreading
p g and transmittingg
•Immunosuppressed cattle may get plaque-like form,
similar to Bowen’s disease in cats, in dogs or in man
BACTERIAL DISEASES
 Mycoplasma bovis
(CPPS – chronic pneumonia and polyarthritis syndrome)
•Mycoplasma bovis pneumonia and in about 10-15% of cases, single or multiple joint M. bovis arthritis with or without
tenosynovitis.

•The lung lesions vary tremendously in extent and severity, starting as growth of M. bovis in bronchioles and bronchi
then coalescing into large areas of yellow caseous like necrosis with invasion and spread via interlobular lymphatics.
Concurrent fibrinous pleuritis also common. Lung lesions can be mixed with other bacterial or viral infections,
especially
i ll Mannheimia
M h i i hemolytica
h l ti pneumonia,i especially
i ll if recentt antibiotic
tibi ti therapy
th was nott carried
i d out.
t

•M. bovis is best confirmed in the suspect lesions by IHC on formalin-fixed tissue. M. bovis can be isolated from most
feedlot lungs, so cultures alone do not confirm the diagnosis, nor does PCR.

•If looked for histologically and immunohistochemically, transient BVD infection is commonly found concurrently and
likely makes the M. bovis lesions more extensive via immunosuppression. Extensive antibiotic therapy may also
promote M. bovis growth and make the lesions more extensive.

•The BVDV lesions may include vasculitis or chronic proliferative arterial lesions in arteries in heart and sometimes
lung, severe atrophy of Peyer’s patches of ileum and occasionally focal areas of lymphocytic myocarditis.

•Immunohistochemistry (IHC) will often but not always

always, confirm BVD virus in these arterial and myocarditis lesions.
lesions
The amount of viral antigen remaining in tissues is often very small and smooth muscle of vessel walls seems to be its
last ‘hangout.’
 Virulence factors for M.
M bovis
•Tissue tropisms vary with strains
•Vsp (variable surface proteins)– rapidly change and
avoid immune system
•Endotoxin like effect via interleukin and cytokine
production
•H2O2 and superoxide derivatives damage host cells
•Suppression
S i off neutrophil
t hil / macrophageh respiratory
i t
bursts
•Immunosuppressive effects
•Compete for nutrients – fatty acids, sterols, arginine
 Mannheimiosis – shipping fever
• Pasteurella hemolytica now called Mannheimia hemolytica and typically causes a fibrino-
fibrino
necrotizing pleuropneumonia.
• ***Feedlot cases which occur after about two weeks on feed often have concurrent transient
BVDV infection resulting in severe immunosuppression.
• B i as a bronchopneumonia
Begins b h i andd passes through
th h stages
t off acute
t bronchopneumonia
b h i with
ith dark
d k
red, swollen consolidated lung tissue and mottled with pale areas of acute coagulation necrosis on
the cut surfaces.
• More swollen, consolidated lung that is dark red and hemorrhagic on cut and pleural surface with
venous thrombi visible is just a more severe and peracute form.
• Later stages and with antibiotic use, many areas will become paler and necrotic, not dissimilar to
the lesions of necrosis caused by Mycoplasma bovis and the two can be mixed together as well.
• The amounts of fibrin on the pleural surface will vary tremendously but usually is abundant and
this fibrin is throughout the interlobular spaces as well on the cut surfaces.
• More chronic and treated cases will have whole lung lobes with gray consolidation and early
stages of pleural fibrin organization.
• W can confirm
We fi theth presence off the
th organism
i in i fixed
fi d tissue
ti by
b IHC andd differentiate
diff ti t it from
f
Histophilus somni, Mycoplasmosis and other bacteria.
• Past multocida causes only a suppurative bronchopneumonia, especially in cases where there is
previous bronchiolar damage. I have yet to see what I would call a primary Past multocida
bronchopneumonia and even if I cultured this organism, I would not consider it as a cause of
death.
 E. coli

• The most common cause of neonatal calf diarrhea

•Other diseases include septicemia,
p , chronic interstitial
nephritis, necrotizing mastitis and pyelonephritis
•Enterotoxigenic (ETEC) strains typically produce only
enterotoxin Sta and fimbrial adhesins F5 (K99) and F41
•Shiga-toxin (STEC) producing strains cause edema
disease in pigs and a polysystemic vascular necrosis
syndrome
d we have
h recently
l identified
id ifi d ini cattle
l
•We do not have IHC for this organism so cultures and
sensitivityy testingg is crucial in outbreaks of ETEC
infections
•Histologically if gut sections are fresh, the mucosa has
masses of organisms on villus brush border enterocytes
 Mycobacterium spp.
• Mycobacterium
M b i bovis
b i isi very uncommon in i North
N h American
A i cattle
l
but does exist in buffalo in Northern Alberta and recent outbreaks
have occurred in elk and cattle in Manitoba in Canada
•Johnes disease due to M M. avium paratuberculosis is a serious problem
in cattle, buffalo and other small ruminants
•There appears to be an association with Johnes and Crohn’s disease
in man
•IHC and/or Fites acid fast stains work well on fixed tissues and is
preferred but the search is still on for the ideal clinical test on live
animals
•Most cases of Johnes are seen in adult cows but I recently confirmed
a case in a one year old feedlot animal in Alberta
•Atypical Mycobacterial skin infections occasionally seen in cattle
Histophilus somni disease
p ((HSDC))
complex

See notes on the next several

slides
i
 H. somni Diseases spectrum
HSDC – “Histophilus somni disease complex”

• Septicemia and sequelae

Thrombotic meningoencephalitis – TME
Myocarditis / pericarditis
Pleuritis
Myelitis
Laryngitis
Arthritis
Nephritis
Multifocal intestinal infarcts
Myositis
Retinitis / hypopyon
• Bronchopneumonia
Part of BRDC
Rare fibrinous bronchopneumonia
Occasionally secondary myocarditis, arthritis and otitis media
• Reproductive losses
Sporadic
S di mastitis,
i i abortion,
b i vagino-cervicitis,
i i i i endometritis,
d i i orchitis,
hi i b balanoposthitis,
l hi i
seminal vesiculitis
Predisposing factors of HSDC

• Stresses e.g. transport, temperature changes, changes

in feed,, respiratory
p y viruses,, overcrowding,
g, handling
g and
processing, etc.
• BVDV immunosuppression not a factor
• Carriers of pathogenic strains important
• Current vaccines are of questionable value
 General characteristics
characteristics,
classification and terminology

• 1956 first described, name H. somni 1969

• 2003 renamed d – analysis
l i off 16S rDNA
DNA and d rpoB
B genes
• Small, gram negative, pleomorphic, nonmotile,
nonencapsulated
p organism
g
• H. ovis, H. agni, H. somni now considered the same
species
• X & V factors not necessary for in vitro growth
• Common surface antigens present in all strains
• Antibiotic therapy
py interferes with isolation
 Virulence factors
• Commensal respiratory & urogenital Tracts
• Nonclinical carriers 3.2 to 8.3%
• IgBPrs – allows intracellular survival, proliferation
• MOMP rapid phase variation – avoid immune system
• LOS - structural and antigenic variation
• LOS - adherence, penetration, IL-1 & TNF
• Biofilm production at sites of adherence promote proliferation
 H. somni Unknowns

• Individual animal susceptibility

• Mechanisms of tissue tropisms
• Mechanisms of reproductive losses
 ITME – Infectious thrombotic meningoencephalitis

• ITME form of H. somni infections seems to be on the increase again in western Canada
and multiple acute deaths over a week or ten days time in a pen not uncommon
• Do not always see tiny hemorrhagic or necrotic foci grossly and can be seen only in
leptomeninges by histopathology. In these acute septicemic cases, lesions of
thrombophlebitis can also be seen in most other tissues submitted for histopathology
• In the above situations however, there will always be a few joints with mild fibrin
chunks or strands seen, and joint fluid is mildly increased and sanguinous or cloudy
• Most cases of HH. somni pleuritis do not have ITME lesions but a few cases of acute
myocarditis cases do. Myocarditis cases will not have ITME lesions
• Whenever a case of ITME occurs, not uncommonly see bilateral laryngeal
necrosis/ulcers/erosions and the typical thrombophlebitis can be seen in these lesions on
histo
• We use IHC to confirm H. somni in formalin fixed tissue, especially in treated cases
where cultures are usually negative
 Histophilus somni myocarditis
• Most consistently results in areas of acute to chronic necrosis of the left cranial and caudal papillary muscles
but multifocal pale foci of necrosis may occur throughout especially the left myocardium as well.
• If chronic, the areas of necrosis may show a zone of purulent material between the necrotic zones and viable
myocardium, and this process is called sequestration and the central free necrotic mass is then known as a
sequestrum.
• Sometimes the sequestrum will be pulled off into the ventricle lumen by the chordae tendinae of the A-V valves
while
hil the
th animal
i l is
i alive
li andd death
d th occurs suddenly.
dd l
• Histologically, the pathogenesis appears to be embolism, but the source is not always apparent, i.e., there are no
pleuritis or ITME lesions.
• Often coexists with a chronic suppurative bronchopneumonia and H. somni can be cultured from the lung and
heart lesions if antibiotic therapy has not recently been extensive.
extensive IHC can be used to confirm the diagnosis and
is done on formalin fixed tissue.
• Occasionally co-exists with Histophilus somni pleuritis but this is not at all common.
• The lung may or may not show passive congestion, depending on whether or not the animal showed congestive
heart failure. Sometimes the animal is found dead with no history of treatment or congestive heart failure signs.
• Acute lesions are hemorrhagic, as in blackleg, and careful examination of the papillary muscles are needed to
make this diagnosis.
• Acute fibrinous pericarditis can also be present, but never without myocardial lesions also being present.
• Sometimes there is vegetative mural or valvular endocarditis lesions as well as myocardial lesions.
• Debatable whether or not vaccination reduces the incidence of.
 Histophilus somni pleuritis
•In feedlot cattle this is seen as often or more often
• than ITME or Histophilus somni myocarditis
•Strains causing pleuritis often do not cause concurrent
bronchopneumonia, septicemia, myocarditis or ITME.
•Death usually occurs very rapidly with animals not seen
sick so are seldom treated.
•The diagnosis
g is q
quite simple
p and differential diagnoses
g
principally include mannheimiosis and Mycoplasma bovis
pleuropneumonia.
•Usually are pure infections with no pneumonia seen on the
cut surfaces of the lung
•Interlobular lymphatic involvement but without pneumonia,
often gives the cut surface a marbled appearance.
 Histophilus somni myonecrosis/myositis

• Occasionally and often along with ITME lesions, large areas of pale necrotic
muscle tissue seen, most often in thigh muscles
• The lesions are quite will defined and vary a lot in size
• May or may not have any hyperemia zones around them, often do not
• C fi by
Confirm b histo
hi t only
l andd cultures
lt nott necessary unless
l no histo
hi t service
i
available
• Important differential is a site of antibiotic injections
• Similar lesions in other tissues such as intestinal serosa and kidneys not rare
 Salmonellosis
•In feedlots, organ involvement usually confined to the intestinal tract, with varying degrees of necrotizing
enterocolitis.
•Outbreaks often occur with several animals involved in one or more pens.
•Lesions are not at all specific and altered in most cases by antibiotic therapy.
•Lesions can be severe with necrotic casts of mucosa and fibrin, especially in the ileum, or may be confined to the
cecum and
cecu a d colon
co o with
w necrosis
ec os s of
o thee mucosal
ucosa surface.
su ace.
•Gross lesions can be similar to coccidiosis, BVDV, and nonspecific necrosis by normal intestinal flora of a mucosa
damaged by some other disease process such as enterotoxemia or sudden alterations in feed.
•Isolation of salmonella sp can be difficult with antibiotic therapy but including mesenteric lymph nodes and gall
bladder as well as tied off intestine can increase the chances. Make sure the lab knows about the antibiotic therapy.
•When outbreaks of salmonellosis occur, make sure you keep in mind that transient BVDV infection may be making
a group of calves susceptible to this organism, so heart, ileum, and a variety of other tissues should be examined
histologically and by IHC to see if this virus may be present. We have run into this situation several times and
remember no gross lesions of BVDV will be seen. “if you don’t look, you won’t find”
•Because of transient BVDV infection, other concurrent lesions may also be present, such as pneumonia.
•Rarely are septicemic forms seen in feedlot situations unless in calves that have just arrived.
•We often use IHC to identify Salmonella sp in formalin fixed tissues and this works well where antibiotic therapy
has been extensive or only fixed tissues submitted
 Arcanobacterium pyogenes

• Originally
O i i ll namedd Corynebacterium,
C b i in
i 1982 renamedd Actinomyces
A i andd in
i
recent years Arcanobacterium pyogenes
• Gram positive pleomorphic rods and histologically always in massive numbers
i suppurative
in i lesions
l i
• Usually a secondary invader via breaks in skin or mucosal integrity then enters
the bloodstream
• Has a protease toxin and factors that prevent local inflammatory responses
• Yellow-green purulent material of variable consistency is typical
• Often a foul odour to the lesions
• Normal inhabitant of respiratory and genital tracts
• Any tissues and organs can be infected
 Fusobacterium necrophorum

• Gram negative anaerobe

• Common inhabitant gastrointestinal tract and thrives in wet, manure-laden
environments
• Opportunistic pathogen that produces an extracellular toxin or leukotoxin
lethal to leukocytes. Leukotoxin aids the development of necrosis and
abscesses
• Also has an endotoxin
• Circulating antibodies do not prevent infection
• Especially a common invader of ulcerative or erosive lesions of the
gastrointestinal
t i t ti l tract
t t andd bacteremia
b t i is
i common
• Navel ill, footrot, liver necrosis, necrotic laryngitis are just some of the
common conditions associated with in cattle
 Clostridium chauvoei myositis - Blackleg

• Most veterinarians recognize the characteristic odour at necropsy; described

as rancid butter odour
• If suspect it, and don
don’tt see typical gas bubbles and dry, dark muscle tissue
anywhere, don’t forget to carefully examine the heart, diaphragm and
tongue muscles
• Mild to moderate fibrinous pericarditis and acute myocardial necrosis
lesions are common in cattle along with skeletal muscle lesions
• Send in suspect muscle for histo and pieces of fresh muscle for Clostridial
cchauvoei
auvoe ddirect
ec immunofluorescence
u o uo esce ce = DIF
• Autolysed carcasses will often show positive for Cl septicum by DIF, but
not Cl chauvoei. Mixed positive results on DIF also common and significant
 Cl t idi
Clostridium perfringens
fi

• PCR has replaced mouse inoculation to identify toxins in tissues and

clinical specimens
• No IHC for most diseases caused by any of the Clostridial organisms
• T
Type A possibly
ibl causes jejunal
j j l hemorrhage
h h syndrome
d
• Type A currently an enigma but associated with tympany, abomasitis,
abomasal hemorrhage and abomasal ulcers in calves

QuickTime™ and a
decompressor
are needed to see this picture.
 Clostridium novyi

• In ruminants
i type A causes myonecrosis,
i type B causes
Black disease, type C is nonpathogenic and type D
causes bacillaryy hemoglobinuria
g
• We occasionally demonstrate in cases of calf abomasitis
and myonecrosis and/or cellulitis secondary to
d h i or castration
dehorning t ti
• We do not have IHC for this organism
 Clostridium septicum
p

• The cause of malignant edema which is now rare due to

vaccines
• Occasionally in sheep, goats, pigs and in necrotizing
abomasitis in young calves
 Dermatophilosis
• Dermatophilosis
p congolensis
g organisms
g found jjust
below or in the stratum corneum as filamentous
organisms but then forms zoospores which are much
more difficult to identify with special stains such as
Gram and Giemsa stains
• Wet, warm conditions conducive to disease and dorsal
trunk regions most often involved in cattle
• Abundant white scales and crusts
• Rarely
R l seen on stains i to invade
i d deeper
d into
i hair
h i follicles
f lli l
• The hyphae type organism is described as ‘railroad
tracks-like’
tracks like with transverse and longitudinal striations
 Staphylococcus aureus

• Necrotizing (gangrenous) mastitis the most common infection

caused by this organism in cattle
• Can be cultured from most skin sites in cattle but especially teat
skin
• Occasionally see udder and teat skin necrosis, vegetative
endocarditis and necrotizing endometritis caused by this organism
 Pasteurella multocida

• We do not have IHC for but we definitely do for

Mannheimia hemolytica
• Not
N considered
id d a primary
i pathogen
h in
i feedlot
f dl cattle
l but
b
certainly plays a role in suppurative bronchopneumonias
• Gross lesions virtually identical to H. somni
bronchopneumonia
• We do not see necrosis or fibrinous exudation associated
with
i h in
i any age off cattle
l
 Anthrax

• Severe outbreaks in western Canada and northern US states

in recent years due mainly to flooding
• Bacillus anthracis is the bacterium involved and is a
federally reportable disease
• We desperately need an antibody reagent for IHC since we
commonly receive only formalin fixed tissues
• Recent cases in Saskatchewan did not have the typical
severe splenomegaly but nasal, oral and anal hemorrhage
were consistent gross findings
 Campylobacter jejuni

• Campylobacter jejuni is currently the leading cause of bacterial

food borne illness in the world
• Very common in the intestinal tract of cattle without illness
• Mild enteritis in calves but not considered a major pathogen
• We have seen several outbreaks of abortion and typically
yp y the
necrotizing and suppurative placentitis is severe
• We have excellent IHC that is specific for this Campylobacter sp.
 Treponema spp
• Treponema brennaborense
b b i the
is h name off the
h organism
i
that causes pastern dermatitis, also known as digital
dermatitis,, hairyy heel warts and ppapillomatous
p digital
g
dermatitis in adult cows
• A Warthin Faulkner stain is needed to clearly see the
organism
i ini pasternt skin
ki sections
ti
• Most often in dairy cows but some cases in beef cattle
• Antibiotics important to treat and topical therapy is
often not effective
 Clostridium tetani

• Our most common tetanus cases are in feedlots

following the use of elastrator bands for castration
 Clostridium haemolyticum

• The
h organism
i is i also
l known
k as Cl.
l novyii type D
• Bacillary hemoglobinuria is the cattle disease
• Recent years commonly seen in adult cattle and feedlot
calves in Alberta
• A soil borne organism
g and often identified in the intestinal
tract of cattle
• Varying degrees of icterus and anemia with
hemoglobinuria characteristic
• Grossly a large area of hepatic necrosis is characteristic
alongg with ggun-metal colored kidneysy
 Streptococcus spp.

• A common isolate in cases of navel ill and vegetative

endocarditis in cattle
• The most common infections in cattle are various
species of Strep. involved in mastitis
 Coxiella burnetii

• Organism
i is i in
i the
h Rickettsiaceae
i k i family
f il
• The cause of Q Fever in humans
• We have excellent IHC specific for and differentiates it
nicely from Chlamydophila sp.
• An important zoonosis and nonclinical carriers common
in domestic ruminants
• We most often see cases of bovine abortion, with
primarily an intercotyledonary placentitis and mild
vasculitis in the placenta
g
• Cattle shed the organism at pparturition and the agent
g is
resistant to drying so spread by wind and dust
 Chlamydophila psittaci

• Recently renamed from Chlamydia sp.

• We most often see in ovine abortions but occasionallyy
cattle as well
• IHC is very specific for on fixed tissues
• A similar placentitis to Coxiellosis
• Maachiavello special stain on placenta works quite well
• Buss
B ss disease in cattle is a fibrino
fibrinouss polyserositis
pol serositis caused
ca sed
by this organism but I have not seen a case
 Leptospirosis

• L. pomona, hardjo and grippotyphosa are most common

in renal disease in cattle but we very rarely see this
disease in cattle
• My experience is only with interstitial nephritis in pigs
and is a problem mainly in slaughter houses where it is
a zoonosis
• I have seen an occasional porcine abortion
• IHC is excellent for L. pomona on fixed tissues
 Actinomycosis - lumpy jaw

• Actinomyces bovis - a very thin, gram positive

filamentous organism
• Common inhabitant of bovine oral cavity and enters via
damage to the mucosa then into mandibular or
maxillary osseous tissues
• ‘Sulfur granules’ are seen grossly in the granulomatous
lesions and these are organisms plus Splendore Hoeppli
material (club colonies)
 Actinobacillosis – Woody tongue

• The organism is Actinobacillus lignieresii,

lignieresii a gram negative
coccobacillus organism
• Also seen in bovine lymph
y p nodes and occasionallyy lung g
• Various locations of the tongue firm and swollen. The cut
surface shows multiple white to yellow, firm, often circular
f i which
foci hi h representt granulomas.
l Adjacent
Adj t granulomas
l can
become confluent.
• Centers of ggranulomas can have small yellow
y foci which
are the sulfur granules
• Easy to diagnose histologically without cultures
PROTOZOAL DISEASES
 C
Coccidiosis
idi i - Eimeria
Ei i sp.
• Eimeria bovis or zurnii in cattle
• Like coronavirus enteritis in young calves, if you don’t open, examine and submit
samples from the spiral colon, the diagnosis is easy to miss
• Similar but milder lesions can be seen in the ileum, but the tissues must be quite
fresh to identify this disease by histopathology of small intestine
• Eimeria bovis is the most common organism and histopathology can easily
make the diagnosis
• The numbers of organisms seen on histopathology is very important since all
feedlot cattle will reveal some organisms on histopathology.They must therefore
be in very high numbers and clearly associated with mucosal epithelial necrosis
• Oocysts are the necrosis-causing stage of the organism
• Sometimes nervous signs seen - ‘nervous coccidiosis’ but no significant
histologic lesions are seen in the brain by histopathology
 Neosporosis - Neospora caninum
•A very important cause of abortions in especially dairy
herds but some outbreaks in beef herds as well
•Coyote and dog fecal contamination of hay in storage
important in the transmission
•Small foci of necrosis with cysts or free merozoites and
inflammatory cells randomly scattered in fetal brain,
l often
less ft in
i heart
h t andd skeletal
k l t l muscle
l
•Rarely see gross lesions in the CNS at postmortem
•We have excellent IHC for, differentiating from
Sarcocystis sp. and Toxoplasma sp.
•Seropositive dams can and often do abort repeatedly
 Sarcocystosis
•All adult cattle myocardial histologic sections have
small to large numbers of cysts,
cysts but rarely is there
visible damage to the myocardium. Much less common
in skeletal muscle tissues
•We
W nott uncommonly l see sarcocysts
t in
i bovine
b i abortions
b ti
with merozoites in various tissues, but most often brain,
placenta and we have IHC specific for Sarcocystis to
differentiate from Neospora
•Interestingly, transiently infected BVDV infected
feedlot cattle often have more myocardial cysts,
cysts
presumably due to immunosuppression
•See the next disease entry for eosinophilic lesions seen
i slaughter
in l ht cattle ttl
 Eosinophilic
os op c myocarditis
yoc d s and
d myositis
yos s

• Causedd in
i most if not all
ll cases by
b sarcocystis
i spp.
• Multifocal areas of yellow-green discoloration in heart and or
skeletal muscles,
muscles often an incidental finding at slaughter or during
necropsy examination
• Sarcocystosis cannot always be proven, even by histopathology
• Presence of large numbers of eosinophils result in the green
discoloration of the lesions
• Appear not to interfere in skeletal or heart muscle function
• We have excellent IHC for, in all species
 Cryptosporidiosis
• Certainly often found in dead neonatal diarrhea calves, but other
infectious agents probably the primary cause
• To see in histologic intestinal sections, it is important to have the
ggut sections fixed veryy fresh, or carefully
y search the sloughed
g
luminal content for the organisms
• The organisms are seen lined up within the brush border of the
tips and sides of villus enterocytes
• Heavily contaminated bedding materials in calving areas often
g
results in higher losses due to this organism
g
• No good treatment for is a problem in outbreaks so sanitation is
crucial
MYCOTIC DISEASES
 Zygomycosis
•Phycomycosis is another older name
•Species of fungus can be Adsidia, Rhizopus, Mucor
and Mortierella
•Common inhabitants of soil, manure and rotting
vegetation, therefore are ubiquitous
•Opportunistic pathogens and antibiotic therapy may
promote their growth
•Most often seen in immunsuppressed cattle in our
experience
•Tropism for vessel walls with necrosis and thrombosis
•Commonly seen in mycotic rumenitis
•Broad, branching, aseptate and irregular hyphae
c
characteristic
ce s c
 Aspergillosis

• Aspergillus fumigatus commonly causes mycotic

abortion with severe pplacentitis and is also a common
cause of mycotic rumenitis, secondary to lactic acidosis
or rumen overload
• Also
Al a ttropism
i for
f vessell walls
ll where
h it resultslt in
i
vasculitis and thrombosis like the zygomycetes group of
fungi
• Easy to identify from the zygomycetes group since
Aspergillus is septate and has parallel sided hyphae
outlines
• Occasionally see generalized infections in feedlot cattle,
likely entering ulcers in the GIT and especially when
immunsuppressed with transient BVDV infection
 Red fescue toxicity and Ergotism

• Ergotamine and ergometrine from the parasitic fungus

Claviceps purpurea and ergovaline from fungi growing
on tall fescue grasses all cause peripheral
vasoconstriction in cattle resulting in digital (and ear,
tail) necrosis
• Losses are higher during cold weather which
exacerbates the arterial vasoconstriction problem
• Must be differentiated from the arteritis of transient
BVDV infections in feedlot cattle which can cause an
identical syndrome
 Dermatophytosis

• Trichophyton
h h verrucosum andd T. mentagrophytes
h most
common species in cattle involved in ringworm
• Especially in younger calves with damp conditions
• Periocular most common site in cattle
• Used oil used to be a common treatment for but lead
poisoning sometimes resulted
• The organism are much easier to find in hairshafts on
skin biopsy sections than in most other species
PARASITIC DISEASES
 Parasitic pneumonia
p
• Not seen commonly in western Canada, due to our drier climate and is caused
by Dictyocaulus viviparus
• When opening lungs, should always be looked for by thoroughly opening the
right dorsal bronchus which extends to the caudal aspect of the caudal lung
lobe
• Can cause AIP in feedlot calves
• Grossly is suspect when a lung shows discoloration of especially the caudal
aspect
p of both caudal lungg lobes. Lungworms
g can result in an AIP type
yp lungg as
well and the mechanism of this interstitial pneumonia remains undetermined
• Sometimes diagnosed histologically by seeing peri-airway eosinophils or even
sections of Dictyocaulus
y larvae in histo sections from caudal lungg sections
• We see it more often now in game farm ruminants such as fallow deer, elk and
roe deer
• Only seen in the fall when the summers have seen abundant rainfall
 Pediculosis
• Veryy common in beef cow-calf herds but onlyy when ppour-on
insecticides have not been regularly or properly used
• Biting lice / Bovicola bovis a much bigger problem than
sucking
ki lice
li / Linognathus
Li h vituli
i li
• Patchy hairloss and visible pruritis should make the producer
susp c ous
suspicious
• Tailhead, inguinal and axillary regions common sites
• Do not rely on to make the diagnosis histologically on skin
biopsies - the chances of seeing lice in histo sections are not
good
 Stephanofilariasis

• In summer months especially, it would be unusual to NOT

see ventral midline patches of alopecia in adult beef cows
d to this
due hi filarial
fil i l nematode
d
• The nematode is Stephanofilaria stilesi
• The intermediate host is the horn fly
• Adult and larvae seen on skin biopsies but sometimes in very
chronic lesions, they can be difficult to find.
 Sarcoptic mange

•Sarcoptes scabiei var bovis and is a zoonosis

•Spread
p byy direct contact and fomites
•Head neck and shoulders then spreads
•Highly pruritic
•Crusts thickening and folding of skin
•Crusts,
•Most often seen in younger calves
•If skin biopsies are examined, it is rare to see the mites in
sections of skin, like in dogs, but the mites are usually
identified on skin scrapings
 Chorioptic mange

•Chorioptic mange - Chorioptes bovis

•Most common mange type in US cattle
•Starts on lower legs then moves up to involve tail folds,
folds
perineal and caudal udder regions
•Crusts, ulcers, alopecia
•Usually large numbers of mites in histologic skin
biopsies
 P l d
Pelodera dermatitis
d titi

• Also known as rhabditic dermatitis caused by free-

living parasite Pelodera strongyloides
• Occurs in cattle when lying extensively on very wet,wet
dirty bedding
• Mainlyy ventral lesions and histologically
g y results in a
severe eosinophilic folliculitis or furunculosis with
nematodes visible most often within hair follicle lumens
• Ventral abdomen and medial thigh regions involved
 Hepatic trematodiasis – liver flukes

• Not common in feedlot cattle but Fascioloides magna can cause

various sized cystic areas containing a jet black pigment with
trematodes
d sometimes
i being
b i difficult
diffi l to find
fi d grossly
l
• Lesions often seen at slaughter and more common in adult cattle
or game farm elk
• Fasciola hepatica and F. gigantica also in North America but
rarely seen in Canadian cattle
MISCELLANEOUS/UNKNOWN
DISEASES
 P3 necrosis in feedlot cattle
• This unique
q entityy in feedlot cattle we first saw in Alberta feedlots in 1996 and cases
have been seen regularly every year since. It has been seen in at least one large NE
feedlot as well.
• Calves arrive off trucks at feedlots and begin to show antibiotic - nonresponsive
l
lameness with
i h 24-72
24 72 hours
h after
f arrival.
i l
• Splitting at the coronary band progresses to frequent hoof wall sloughing in 2-4 weeks.
• Cases are usually sporadic but up to 20% of lots of calves have been seen and these are
usually from the same farm of origin
origin.
• I believe this to be a multifactorial disease but reduced arterial blood supply to P3 and
the distal soft laminae is the ultimate cause (P3 infarction). Reduced blood flow while
calves
ca ves are
a e standing
sta d g on
o hard
a d surfaces
su aces for o prolonged
p o o ged periods
pe ods of
o time
t e we think
t iss
responsible. The medial digital artery is the one suspected of being responsible.
• Dehydration and anything that reduces cardiac output can be contributory.
• Transient BVDV vascular lesions in the myocardium
y is often found if looked for
histologically but this has to be proven to reduce cardiac output in these cases.
• Secondary bacterial infection occurs once the soft laminae swelling causes the sole and
hoof wall to split open at the white line.
• Low environmental temperatures is perhaps contributory in a low percentage of cases.
• Differential diagnoses include footrot, acute laminitis, primary frostbite, ergotism and
fescue foot. We have ruled out all of these in our P3 necrosis cases.
 Urethral obstruction - urolithiasis
• In cattle the site of obstruction is most often the sigmoid flexure of the penis
• Not in all cases are uroliths found; sometimes only masses of soft necrotic
debris and fibrin are found and these may represent mucosa that has been
damaged and sloughed by a passing urolith or areas of necrotizing cystitis
• To examine the entire urethra properly, requires opening the pelvis. To easily do
this, split the symphysis then cut the shaft of the ilium on one side and pull the
pelvis open with your hands
• Associated with ventral rupture of urethra resulting in subcutaneous/fascial
urine collections or ruptured bladder with urine collecting intra-abdominal.
• A local or diffuse peritonitis may be present if the bladder is ruptured and
bacterial contamination is also present
• Often accompanied by varying degrees of hydronephrosis within renal lobules
 AIP – Feedlot interstitial pneumonia
•Commonly seen in feedlots and often in animals that are nearly finished or at least late in feeding periods.
periods Lots of cases seen in animals
in earlier feeding periods as well.
•****A poorly understood entity is an understatement.
•Should be thought of as a syndrome rather than a distinct disease entity since likely a variety of and mixture of causes can lead to the
similar end-stage lesions.
•Important
I to realize
li that
h theh meaty, brown
b colored,
l d rubbery
bb lobules
l b l seen most consistently
i l in
i the
h caudal
d l lung
l lobes
l b isi a combination
bi i off
hyaline membranes and pneumocyte II hyperplasia and occurs because of acute necrosis of type I pneumocytes, the flat lining cells of the
lung alveoli. Epithelial cells of terminal airways-bronchioles are involved in this process as well = Clara cells. It is cellular proliferation
and the protein content of the hyaline membranes and alveolar edema fluids that makes the lungs so heavy.
•Edema and emphysema are features of but varies in severity tremendously from case to case. Finding emphysema alone in a bovine lung
sho ld never
should ne er be the criteria for calling a lung
l ng interstitial pne
pneumonia
monia since it can occur
occ r rapidly
rapidl during
d ring terminal respiratory
respirator exertion
e ertion even
e en in
normal lungs. This is true for interlobular and bullous emphysema, but usually not subpleural emphysema.
•Typically the lung is rubbery throughout most lobes but most consistently in caudal lobes. The lungs are mottled due to intermingled
meaty, firm, lobules and yellow, aerated lobules which appear more normal.
•Airway exudates not seen on cut surface unless concurrent bacterial bronchopneumonia also present but a ‘bronchiolar pattern’ can be
presentt andd extending
t di back
b k into
i t the
th caudal
d l lobes,
l b especially
i ll if BRSV isi suspected
t d as a predisposing
di i or solel cause. This
Thi bronchiolar
b hi l pattern
tt
is usually seen histologically as bronchiolitis obliterans.
•In my opinion, 3 methyl indole from rumen fermentation of tryptophan is partially responsible for the pneumocyte I necrosis but the lung
is predisposed to this by some previous or concurrent lung disease, especially bronchiolitis -causing entities, such as BRSV. The
compartmentalization of the bovine lung and abnormal ventilation/perfusion ratios likely also play a role but the disease has not been
experimentally reproduced to be able to determine the exact mechanisms.
mechanisms
•Pulmonary hypertension with cor pulmonale is often the cause of death but in acute onset cases, simple hypoxia from respiratory failure
also is important.
•If you are going to submit fixed lung for histologic examination, important to take at least five sections from upper, lower, cranial and
caudal parts of one or both lungs. If tiny bubbles of subpleural emphysema are visible, important to take sections from these areas, since
they give us the best chance of finding BRSV or other primary infectious causes on IHC. IHC
•Bovine lungworm infection often terminates in AIP in feedlot situations as well.
•Interestingly, in Alberta feedlots 80% of all cases are in heifers and heifers are always given growth-promoting implants
Cardiac failure
• Left sided heart failure (due to myocarditis, myocardial necrosis,
cardiomyopathy, mitral/aortic valve disease, congenital heart diseases)
– Acute = pulmonary congestion
congestion, edema
– Chronic = chronic lung congestion, chronic edema, heart failure cells,
fibrosis
– Chronic form often results in both left and right failure due to pulmonary
hypertension
• Right sided heart failure (due to pulmonary hypertension, cardiomyopathy,
tricuspid and pulmonary valve disease, congenital heart disease)
– Acute = enlargement and congestion of spleen and liver, sometimes
mesocolonic edema
– Chronic = nutmeg liver, edema, ascites
• Cor Pulmonale - right heart failure resulting from severe lung disease
resulting
g in p
pulmonary
y hypertension
yp
– Particularly common in the bovine species because pulmonary
hypertension readily occurs in cattle
 Abomasal ulceration
• Commonly seen in various sizes, numbers and distribution in the abomasum in
feedlot cattle. Often an incidental finding with no good explanation found
• Seen in all ages of cattle but most financial losses are 1-3 month old healthy
calves with perorated ulcers, peritonitis and sudden death
• Can be very small, hemorrhagic and acute or can be large, irregular, pale and
chronic
• Most of the time BVDV is suspected but a workup on large numbers of cases
often does not confirm this
• The abomasal mucosa is thin with minimal supportpp stroma and focal ulcers
can occur easily, due to increased gastric acid output, which occurs in stress.
These are often hemorrhagic in acute stages, until granulation tissue
production occurs in the depth of the ulcers
• Helicobacter sp. not a factor like gastric ulcers in man
• Pepsinogen and HCl acid both are damaging to mucosal epithelium
• Ulcers very seldom perforate in feedlot cattle as they do in young beef calves
on pasture
 Omasal leaves necrosis
• E
Extensivei necrosisi off omasall leaves
l is
i not uncommon in i feedlot
f dl
cattle and a cause is not always found
• The fact the leaves have a free border means they are sensitive to
ischemic damage, such as fungal invasion and vascular
thrombosis, cardiac insufficiency, BVDV damage to epithelium
and/or
d/ blood
bl d vessels l andd secondary
d to
t ruminal
i l acidosis.
id i
• Disseminated intravascular coagulation = DIC can be
responsible
p as well by
y blocking g small blood vessels with fibrin
microthrombi.
• If a history of extensive antibiotic use, mycotic vasculitis by
Z
Zygomycotic ti fungi
f i would ld be
b my first
fi t differential.
diff ti l
• ****Unfortunately, the omasum is seldom opened at
ppostmortem. The omasum is often not enlarged g at all in such
cases.
 Laryngeal
y g ulcers, erosions, necrosis
• Commonly we see laryngeal lesions in feedlot cattle at postmortem and especially co-
existent with various lung infections
• Usually secondary or develop concurrently with lung disease but once ulcerated and if
laryngeal ulcers are secondarily infected, can seed the lung with an aspiration or
gangrenous pneumonia due to a mixture of gram negative and positive anaerobes, or an
aspiration type Arcanobacterium pyogenes bronchopneumonia
• H.somni septicemia cases often results in thrombophlebitis in the larynx with acute
vocal fold or arytenoid cartilage necrotic lesions. These are always bilateral and can be
quite small initially. These quickly become secondarily infected
• Severe coughing can probably initiate laryngeal erosions just due to the vocal folds
slapping together and these are called contact ulcers
• Mycoplasma bovis likes to grow in laryngeal ulcers and these progress in size once
involved. This is because the organism will grow readily in tissue damaged by some
other organism or mechanism, at a time when they are present in the bloodstream
(bacteremia)
 Bronchiectasis
• Means a cranial ventral lung distribution of abscess – like structures with purulent
exudate grossly surrounded by a thin to thick fibrous-like wall.
• This is not a cause of death,, it only
y needs to be interpreted
p at ppostmortem as suggesting
gg g
chronic, slow-progressive bacterial bronchitis by pyogenic type bacteria.
• Represents airways, mainly bronchi, which have a chronic, slow-progressive growth of
pyogenic bacteria that eventually destroys the wall of the airway in a centrifugal manner
andd the
h lumens
l are filled
fill d with
i h purulent
l material.
i l
• May project as nodules above the surface of the pleura and the lung parenchyma itself is
dark red to purple and collapsed.
• An thing that initiates a bronchitis and bronchiolitis such
Anything s ch as PI3 virus,
ir s BRSV,
BRSV IBR virus
ir s
and perhaps other respiratory viruses can lead to bronchiectasis. These viruses are the
most common initiators of bronchiectasis.
• Mycoplasma bovis infection in CPPS cases often start out as a bronchiectasis but
continue to spread and adjacent lesions coalesce to result in larger areas of coagulation
necrosis and sequestration. The wall of the airway is not as easily seen in CPPS
bronchiectasis like it is with other pyogenic bacteria involved, such as Staph,
A
Arcanobacterium
b t i andd E coli.
li M.
M bovis
b i should
h ld nott be
b thought
th ht off as a pyogenic
i organism.
i
• These nodular lesions often can grow to 1 cm diameter or more.
 Bronchiolitis obliterans
•A diagnosis made histologically in especially feedlot
cattle lung tissue
•Occurs when there is partial destruction of bronchiolar
epithelium with fibrin being replaced by fibrous
ti
tissue/granulation
/ l ti tissue
ti
•In-growth of fibrous tissue into the bronchiolar lumens
results in partial obstruction with the more distal
alveolar parenchyma being collapsed
•Commonly seen with PI3, IBR and BRSV virus
infections in late or resolved stages
•These airways are common sites for Mycoplasma bovis
growth in CPPS cases in my opinion
•If
If no secondary
d i f ti then
infection, th collapse
ll andd lung
l
congestion are the only gross lesions seen
 Pulmonary emphysema
• Three types seen grossly- bullous, an exaggerated form of
i
interlobular
l b l emphysema,
h interlobular
i l b l andd subpleural.
b l l A fourth
f h
type, alveolar emphysema is seen in chronic obstructive
ppulmonaryy disease but is mainlyy a histologic
g diagnosis
g
• Finding interlobular or bullous emphysema do not constitute a
diagnosis of interstitial pneumonia by itself, since it can occur in
an case where
any here animals die with ith terminal respiratory
respirator distress
• Subpleural emphysema occurs where bronchioles are partially
obstructed byy exudate or bronchiolitis obliterans,, a chronic form
of necrotizing bronchiolitis. BRSV commonly shows subpleural
emphysema, both in phase I and localized areas of phase II lesions
 Liver- infarcts or large areas of necrosis
• Hepatic infarcts are often dry, putty colored or yellow areas of dry type necrosis
surrounded by narrow zones of hyperemia. Of various sizes and randomly scattered
throughout the liver.
• These are either due to Fusobacterium necrophorum and arise embolically from an
ulcerative rumenitis or focal intestinal ulcer or, and even more often in our experience,
are due to fungal elements invading vessel walls and causing thrombosis of hepatic
arteries and veins.
veins These are originating from ulcerative lesions somewhere in the GIT
and often no rumenitis lesions are found. The history often includes extensive antibiotic
therapy and if one goes looking for the lesions, BVD vasculitis in heart and other tissues
is often found. Immunosuppression therefore, often plays a role in feedlot cattle.
• Necrosis of leaves of the omasum is not an uncommon finding and can be the source of
the fungal elements. Members of the Zygomycetes group Absidia, Rhizopus or Mucor are
usually involved.
• Histo alone can differentiate between these two etiologies of F. necrophorum and
mycoses.
• Occasionally large single infarcts are seen which can be due to Cl. hemolyticum but
hemolysis and hemoglobinuria are usually present as well well, resulting in hemoglobinuric
nephrosis (bacillary hemoglobinuria).
 Honker’ss syndrome – tracheal hemorrhage and edema
Honker
• Acute onset of respiratory distress with stertorous respirations or sudden death
in respiratory distress.
• Severe submucosal edema and/or hemorrhage of the cervical trachea along
with congestion, hemorrhage and edema of peri-tracheal tissues.
• Usually lesions not distal to the thoracic inlet.
inlet
• Occurs in cattle nearing market weight and no predisposing causes known.
• Mechanisms of edema, hemorrhage unknown.
• Extensive histopathologic and immunohistochemical workup has not supplied
any answers as to cause.
• Some cases have an inflammatory component and squamous metaplasia of the
tracheal epithelium is occasionally seen. The significance of these findings is
not known.
• Significant lung disease usually lacking.
 Pulmonary fibrosis
•Most
Most often found at slaughter in adult cows
•Develops in two ways: 1. organization of fibrin or
repetitive severe or persistent damage to endothelial cells
or type
t I alveolar
l l epithelial
ith li l cells
ll 2 persistent
2. it t
inflammatory changes of alveolar walls
•Can be well developed within 14 days
•Feedlot cattle that survive AIP is a common cause in my
opinion
•High
High mountain disease in adult cows another cause
•Chronic allergic pneumonia another cause
•Cases seen in slaughterhouse specimens are idiopathic
•Often
Oft resultslt in
i congestive
ti heart
h t failure
f il and/or
d/ cor
pulmonale due to pulmonary hypertension
 Disseminated intravascular
coagulation=DIC
•Most textbooks use the term consumption coagulopathy
synonymously l with
i h DIC but
b I think
hi k we as histopathologists
hi h l i can
make the diagnosis histologically before a hemorrhagic diathesis is
seen grossly
•Seeing ‘shock
shock bodies’
bodies in small vessels in multiple tissues to me
suggests this diagnosis
•In all large animals DIC is associated with sepsis, neoplasia, GIT
disorders renal disease and hemolytic anemia
disorders,
•A whole spectrum of single tissue ischemic organ failure occurs
which can include hemorrhagic diathesis
•Single
g organg failure with DIC is more common in large g than small
animals
•Renal cortical necrosis may be a good e.g. of single organ failure
with DIC and saddle thrombosis of the terminal aorta another
 Polysystemic
yy vascular necrosis
•This is a new disease entity of unknown cause but may be
associated with a particular strain of E. coli
•Cases
Cases can be sporadic or there is high morbidity and mortality
especially in young calves
•One herd in Southern Saskatchewan experienced a loss of 15
calves out of 100 cows in one one month period
•The lesions occur in multiple numerous tissues and are a non-
thrombotic, necrotizing arteritis that are subacute to chronic but are
dramatic and seen even at low-power microscopy
•In the brain the lesions are associated with large areas of
hemorrhage
•Tissues most often with lesions are intestine, forestomachs and
kidneys
kid
•Currently the thinking of a group of pathologists is this is the
equivalent of Edema Disease as seen in pigs and may be caused by
a Shiga-type toxin of specific E.
E coli strains
•Mainly in young calves while sucking on the cows but an
occasional adult case has also been seen
An unknown
unknown, high morbidity and high
mortality necrotizing enterocolitis

•In the last several years, we have seen a few herds with a calfhood
neonatal fatal diarrhea with a high morbidity and mortality in which
we have
h bbeen totally
ll unable
bl to establish
bli h a cause despite
d i thousands
h d
of dollars spent on diagnostic testing
•The lesions throughout the intestinal tract look viral but all
attempts at isolation,
isolation IHC and clinical workup have totally failed to
identify a cause.
•The initial herd lost 150 out of 200 calves by three weeks of age
•The
The month of March and April is when these outbreaks occurred
•Some unknown virus is strongly suspected
•We have seen this disease in four herds in Alberta so far
 Fat necrosis-adult
necrosis adult cows
• Mostly involving the abdominal fat stores, such as in the
mesentery, perirenal,
i l etc
• Hardening of the fat causes ureteral or intestinal obstruction or
other organ dysfunctions
• Possibly a number of causes but the pathogenesis is not clear
• Also called lipogranulomatosis
• Acute to chronic inflammatory changes with giant cells and
fibrosis in chronic stages on histopathology
• The
Th necrotic i fat
f has
h a deep
d yellow
ll colorl
• Persistent pyrexia suggested as a common cause
 Middle uterine artery rupture
• Adult cows found dead with bleeding out into the abdomen from
a ruptured aneurysm of a uterine artery
• Copper deficiency one possible cause due to its role in elastic
fibers development but idiopathic cases seen as well
• Possiblyy more commonlyy seen in horses
• Other causes of uterine artery rupture in cattle include uterine
torsions or prolapses
 Acute post-vaccination deaths

•Anaphylaxis with severe pulmonary and laryngeal

edema sporadically
p y seen and well known but we have
had at least one herd where the vaccinations were given
with an automatic type vaccination gun and accidental
intra jugular vein injections resulted in multiple acute
intra-jugular
deaths of young calves.
•Careful dissection of these cases is required to find the
needle holes in the jugular vein walls
 Neonatal pulmonary vasculitis
and/or
d/ h hemorrhage
h
•Of the 1600+ neonatal calves I did histopathology on in the beef productivity study,
I saw about 150 cases of this new entityy
•Mainly in stillborn or neonate nonviable calves, occasionally in near-term aborted
fetuses
•One or multiple pulmonary arteries of various sizes with tunica media necrosis or
mixed with hemorrhage g or with subacute to chronic mixed cell inflammatoryy
changes
•In acute cases, hemorrhage into adjacent alveolar lumens often seen as well
•Thrombosis not a feature and except for occasionally in the heart, there are
definitelyy no vascular lesions in other tissues
•I suspect it has something to do with in utero nutritional deficiencies, possibly
related to Vit E deficiency but proof is so far lacking.
•It is my impression there is incomplete development of lung vascular smooth
muscle cells based on routine H and E sections, numerous special
p stains and IHC
stains done
•IHC workup on numerous cases for all infectious agents we are capable of doing
have all been negative
•Nothingg like this has been described in human neonatal ppathologygy texts or literature
•So-called neonatal pulmonary hypertension may be somehow associated
•In trying to establish a cause it is important to remember that pulmonary arterial
pressure suddenly increases ten-fold at birth
 Idiopathic
p hairloss
•This is a common condition in many beef herds in western Canada
and producers always think lice or other external parasites are
involved
•The cause has not been determined and also is common in horses
•Biopsies show follicles to all be in telogen, but without new hairs
growing
i in i deeper,
d unlike
lik so-called
ll d telogen
l defluxion
d fl i or effluvium
ffl i
as seen in dogs and cats
•Most often seen in spring, February through to May and no
treatment helps
•Some herds get it every year while others never have the problem
•Nutritional problems have not been identified
•Pharmaceutical
Pharmaceutical firms usually end up paying diagnostic bills
because vets and owners are convinced these are parasiticide failure
cases
•Rarelyy are external parasites
p found
•Most often seen in adult cows and bulls
 Jejunal hemorrhage syndrome
• Also called hemorrhagic bowel syndrome
• Most often seen in adult dairy cows but beef cows and
occasionally feedlot cattle cases seen
• Circumstantiallyy associated with Cl. Perfringens
g type
yp A
• Localized massive intraluminal hemorrhage into the
proximal jejunum with obstruction by large blood clots
• Histologically
i l i ll extensive i areas off mucosall necrosis
i with
ih
massive hemorrhage but no vasculitis or primary infectious
g
agents are seen
• Varying degrees of paralytic ileus
• Very low morbidity but high mortality
• Some herds experience numerous cases
 S ddl th
Saddle thrombosis
b i off aorta
t

•We see sporadicdi cases off this

hi in
i calves
l younger than
h six i
months of age
•The cause is not known but the location of origing of the
umbilical arteries from the external iliac arteries has
been proposed to somehow be related
•Get posterior paralysis with cold limbs like the disease
in dogs, horses and especially cats
•The history often includes having diarrhea, or having
b
been treated
d ffor scours or being
b i otherwise
h i just
j sicki k for
f
one to two days previous
•Sometimes histologic g evidence of DIC is seen in other
tissues
 Osteochrondrosis - OCD
• Cattle most often involving distal condyles of femur with chronic ulcerative lesions or
flaps of cartilage lifting off
• Also seen in pigs
pigs, horses,
horses dogs
• Usually chronic lameness part of history
• Often an incidental finding if routinely open stifle joints and don’t confuse with a
chronic septic arthritis which has resulted in ulceration of articular cartilage due to
chronic bacterial infection
• In young game farm bison, severe copper deficiency results in a severe form,
especially in the stifles
• Usually bilateral lesions present
• Don’t confuse chronic OCD lesions with normal articular fossas, which are normal
not-weight bearing areas of several joints
• Other sites include lateral trochlear ridges, humeral heads, distal radius, elbow, tibial
tarsal and occipital condyles
• Common in adolescent bulls
• P b bl genetic
Probably i andd nutritional
i i l factors
f
• Essentially is a defect in endocartilagenous ossification
 Pyelonephritis

• In feedlot cattle, may or may not be co-existent with urolithiasis

• Often some degree of cystitis present and is the source of infection which has
ascended the ureters
• Very large variation in degrees of severity in terms of amount of kidney
parenchyma involved, especially in feedlot cattle. If severe, it can be the cause
of death, but often is an incidental finding at PM
• Usually pale foci visible first on the cortical surfaces and important to open the
kidney longitudinally in order to see all regions, including medullary and pelvic
regions of the kidney. Elongated pale streaks of necrosis and sepsis seen
extending from the pelvis out to the cortical surfaces
• Little value in spending money on cultures and Corynebacterium renale or E.
coli most often involved
• May be cause of death if severe enough, or concurrent with other disease
processes.
 H d
Hydronephrosis
h i
• Urolithiasis the most common cause of hydronephrosis in feedlot
cattle but usually is not severe and not the cause of death
• May be unilateral and not significant as a cause of death if the other
kidney is normal. The contralateral kidney will often show
compensatory hypertrophy if this occurs
• A congenital form is occasionally seen in feedlot cattle and can be so
extensive that chronic renal failure occurs as the animal grows
• Severity varies from dilatation of renal pelvic areas only to loss of
medullary tissue to loss of all of medulla as well as much of cortical
tissue. Some but not all lobules in a bovine kidney can be variably
involved, especially in the congenital form
• Concurrent ureter dilatation often seen
 Chronic interstitial nephritis
p or ‘white spotted
p kidney’
y
in calves
• Most often seen as an incidental finding at postmortem in calves up to four
months of age
• Is a multifocal, nonsuppurative interstitial nephritis with earlier stages seeing
‘microabscesses’ with neutrophils and cell debris in tubule lumens
• O
Occasionally
i ll E. E colili is
i isolated
i l t d from
f the
th lesions
l i but
b t this
thi is
i the
th only
l prooff off its
it
involvement
• Seldom manifest as clinical urinary disease; often an incidental finding at
necropsy, exceptt in
i younger calves
l on pasture
t or while
hil still
till in
i calving
l i pens in i
younger calves, where it can be so severe that chronic renal failure occurs
• Lesions are due to a previous bacteremia, thought to be most often E. coli but
S l
Salmonella
ll sp andd Leptospires
L t i also l suggestedt d as causes
• Often randomly distributed, raised, firm white foci and often dramatic grossly
• Lesions are often misinterpreted as neoplasia
• Lesions in kidneys multifocal to diffuse and often resemble neoplastic processes
 Renal cortical necrosis
• Varying degrees of acute to chronic necrosis of kidney cortex associated with a wide variety of
diseases which result in hypotension
yp or hypovolemia
yp and associated shock.
• Cases of multiple infarcts may actually often be this entity since with the bovine kidney being
lobulated and thus compartmentalized, cortical necrosis can be multifocal rather than diffuse. With
cortical necrosis however, no conical shaped areas of necrosis are seen on cut surface like in true renal
infarcts due to embolic vascular obstruction
obstruction.
• Usually lines of demarcation between viable and necrotic kidney tissue are obvious and may involve
an entire kidney or large local areas only, similar to renal infarcts. The cortical capsular surfaces can be
very coarsely mottled and it is important to open the kidneys transversely or longitudinally to make this
diagnosis.
diagnosis
• Cases have been seen in severe bacterial toxemias, white muscle disease, clostridial disease,
necrotizing enteritis, hardware disease and grain overload, to name a few.
• Severe anemia and dehydration can result in acute renal cortical necrosis.
• Sometimes histopathology on the kidney needed to confirm but seldom identifies a cause.
• 40% of arterial blood passes through the kidney cortex and makes them particularly susceptible to.
 Posterior vena cava thrombosis
• Feedlot cattle should be opened with the left side down with the head to the right and
hepatic abscesses and noncollapsed mottled lungs should give a clue to this disease. The
vena cava over the
h dorsum
d off the
h liver
li should
h ld beb openedd before
b f the
h viscera
i are removedd
to confirm the diagnosis. This is best done by hand, without a knife. Pull the dorsal
aspect of the liver down and this will expose the vena cava where it runs below the
kidneyy over the dorsal ppart of the liver then ppasses through
g the diaphragm
p g
• Then open the vena cava where septic thrombi and abscesses are found
• Occasional the liver septic thrombi are in large, deeper veins in the liver
• Septic emboli, abscesses, thrombi and pulmonary ruptured aneurysms are often visible
with septic areas throughout all lung lobes. If an aneurysm has ruptured in the lung, the
large airways and trachea should contain large amounts of blood clots and the rumen
often contains clots that have been swallowed. If the vena cava is thrombosed, ascites
may also
l beb presentt
• Often no ruminal lesions of rumenitis at the time this syndrome occurs
• May be found dead or show respiratory signs for several days prior to death. Dairy cows
are often found dead in their stalls with blood clots in the mangers
• Sometimes sudden death occurs with extensive septic embolism in lung seen only with
histologic sections
 Posterior vena cava syndrome lung lesions
•Lung lesions are randomly distributed throughout most lobes but especially caudal lung
lobes.
•Lesions vary from mixed gas-filled and purulent areas, septic thrombi, large areas of
hemorrhage due to ruptured aneurysms and in these latter cases, large blood clots are in the
large airways. The lungs are pale if the animal bled out and swallowed large amounts of
blood.
•Vegetative endocarditis of the right side of the heart resulting in showering into the lungs
may look
l k similar
i il but
b t gas producing
d i organisms i are nott involved
i l d andd aneurysms rare.
Abscesses and thrombi are more likely and are often seen only histologically.
•In cases with aneurysms, aspirated blood into lung lobes occurs resulting in hemorrhagic
areas which are often visible on the pleural surface.
•Don’t forget to carefully examine the liver for abscesses and especially the vena cava (pvc)
where it passes dorsally over the liver, passes through the diaphragm, and dumps into the
right atrium of the heart. This is easiest to do before removing the abdominal viscera.
Simply pull the dorsal aspect of the liver down or ventrally with your hands and this can
only be done if the carcass is lying with its left side down. This exposes the vena cava as it
traverses over the liver.
•The lung lesions can be severe and the liver lesions relatively minor if one abscess that has
eroded into the PVC happens to continually shower septic emboli to the lung over a long
period of time.
 Acute ruminal tympany - Bloat
• A difficult ggross diagnosis
g to make in many y cases due to co-existence of other
diseases, lack of all of the typical expected changes concurrently, and varying degrees
of postmortem autolysis.
• In my opinion, gas type bloat does not kill cattle, only frothy bloat does.
U f
Unfortunately,l in
i many cases the h ruminal
i l foam
f has
h dissipated
di i d by
b the
h time
i the h
postmortem is done or only small amounts remain and it is then difficult to decide.
• Classic changes include: 1) cranial carcass congestion and caudal pallor. 2)varying
degrees of flank fold fascial and subcutaneous edema 3) liver and kidneys very pale 4)
right heart often dilated with little ventricular clotted blood 5) lungs bilaterally
collapsed and congested 6) tracheal mucosal studded with petechial or diffuse
hemorrhages but no blood clots 7) typical bloat line at the thoracic inlet but a common
finding in many conditions and should not be used to make the final decision 8)
intense congestion of meninges, brain, paranasal sinuses with hemorrhage 9)
enlargement and congestion of prescapular lymph node and small, very pale
prefemoral lymph node.
• ***I routinely will take histo sections of especially caudal lung lobes and look for
intense hyperconstriction of pulmonary vascular smooth muscle. This is not
pathognomonic for bloat but is consistently present even in cases with lots of
autolysis. In lends support to my necropsy bloat diagnosis. This is not found in
textbooks of pathology or taught in pathology classes or lectures.
 Acute abomasitis

• More common in younger calves on pasture but occasionally

hemorrhagic, necrotizing and emphysematous abomasitis with
varying degrees of edema seen in feedlot calves, sometimes co-
existent with other diseases including enteritis or colitis
• Clostridial agents often isolated but difficult to establish if these
are primary due to invasion through previously eroded or
ulcerated areas, or are just postmortem invaders
• Can be seen along with necrotic omasal leaves and rumenitis
lesions secondary to chronic or subacute lactic acidosis
• Often idiopathic and no cause established
NUTRITIONAL DISEASES
 Iodine deficiency
•Goiter or enlarged thyroid glands is seen in many species but
not commonly now since iodized salt free choice is standard
management practice
•But just because a newborn bovine does not have goiter does
not necessarily mean it has normal thyroid function
•Subclinical
Subclinical selenium deficiency can reduce circulating T3
levels which is more active than T4 - see the text information
on the next slide
•There may be other nutritional or metabolic factors involved
in utero, similar to dysmaturity syndrome in foals, that we as
yet do not know about
 Neonatal thyroid
y ggland
malfunction of unknown cause
•More than 200 cases in the western Canada beef productivity study had
abnormalities of the thyroid glands of aborted, stillborn or neonatal
nonviable calves without any visible goiter
•Because
Because the thyroid gland was a tissue that was required to be submitted,
many veterinarians observed these glands, although of normal size, to be
abnormally pale or were both smaller than normal as well as paler than
normal
•The following photos show the variety of abnormal thyroid glands
histologically without goiter being observed grossly
•In utero colloid production and normal thyroid gland function begins at five
months gestation so calves with these abnormal thyroids at birth would have
low metabolic rates and thus not survive in most cases
•Perhaps subclinical selenium is responsible in some of these cases but
obviously
b i l a lot l t or researchh is
i needed
d d on this
thi andd there
th is i probably
b bl other
th
toxic, metabolic or deficiency factors involved
 Vitamin E & Selenium
•In our part of the world, Vit E is just as important as selenium in nutritional
myopathy, especially in newborn calves
•Colostrum
Colostrum is the calf
calf’ss primary source so feed levels and pregnant cow
supplementation is very important and may play an important role in weak
calf syndrome
•Vitamin E functions:
•1. An antioxidant to neutralize free radicals
•2. Enhances both humoral and cell mediated immunity
•3. Increases Vit C production
•4. Inhibits platelet aggregation
•5. Preserves endothelial cell function
•6. Preserves normal function of leukocytes, especially neutrophils and
monocytest
•I saw many examples of poor inflammatory cell function in adult cattle in
the study
•In
In addition to muscle and heart functions in later weeks of calfhood,
calfhood Se
may play a role in normal in utero thyroid function in fetuses and newborn
calves and help prevent weak calf syndrome
 Nutritional myopathy
• Vitamin E/Selenium deficiency is responsible and the classic picture is fast-
growing calves that die suddenly or become acutely stiff and recumbent
• Vit E most often in very young calves, including neonates, abortions,
stillbirths and often do not have much mineralization as in selenium deficiency
so not as visible histologically and therefore usually not suspected grossly
• Best tissues are heart, tongue, diaphragm and other active muscles such as
thigh muscles
• N t having
Not h i any gross lesions
l i does
d nott rule
l it outt so muscle
l for
f histopathology
hi t th l
is important, and liver for Vit E / Se analysis. Submission and collection of
serum for Vit E analysis has very strict requirements
• M l can be
Muscles b involved
i l d with
ith no heart
h t lesions
l i andd vice
i versa as well
ll
• Adult cattle can have nutritional myopathy as well as other lesions, especially
if Vit E deficiency is responsible
 Polioencephalomalacia
• Two forms seen:
• 1) on high grain rations with cerebral cortices only involved-most feedlot cases
• 2) on high sulfate water (alkali) in adult cows, usually on pasture
• The #2 type often shows hemorrhagic areas of the thalamus on cut surfaces of
the brain, as well as having some usual cortical involvement
• Polio now determined to be due high sulfur and resulting sulfide production in
the rumen, not thiamine deficiency
• No other condition results in positive Wood’s lamp fluorescence on the cut
surface of involved cortices and this works on formalin fixed tissue as well
• Gross lesions often only subtle yellow discoloration of especially sides and
depths of sulci, more-so than tops of gyri. Using a hand-held magnifying lens
can help identify these lesions in cases with subtle lesions
• H2S is produced by ruminal bacteria and sulfide readily crosses the blood-brain
barrier where it interferes with carbohydrate metabolism of brain cells
• Little evidence now for true thiamine deficiency even though it is successful in
therapy - but this benefit is nonspecific
 Starvation/primary malnutrition
•Protein-energy
Protein energy malnutrition common in Canada due to our long
winters and periodic dry summers with poor quality winter forages
often fed
•Grain straw is often relied on to winter cattle on poorly managed
farms and if a winter is especially long and cold, the TDN content
is not high enough especially for pregnant cows and growing cattle
•Lack of body fat stores and serous atrophy of fat are the typical
lesions, but concurrent chronic disease processes must be first ruled
out
•Long-bone bone marrow serous atrophy is the last site for serous
atrophy
t h to t occur andd pericardial
i di l andd perirenal
i l fat
f t stores
t are secondd
most common sites for serous atrophy
•In our experience pregnant cows can starve to death yet have in
utero fetuses with normal body fat stores
 Abomasal impaction
•Common in adult cows due to long, g, cold winters and
finely chopped, poor quality roughage being fed
•Can also occur along with omasal and ruminal impaction
secondary to vagus indigestion (20% of cases)
•Inadequate water intake especially in winter months
predisposes to impaction so reliable water sources
important
•Very sandy soil areas where sand is ingested along with
gground forage
g can cause this pproblem as well
•Especially common in pregnant beef cows where low
TDN forages along with competition for abdominal space
are factors
TOXICOLOGIC DISEASES
 Monensin toxicity
•Is one of the ionophores in cattle production used to
promote growth and improve feed efficiency
•Also a coccidiostat
•In ruminants causes equal damage to cardiac and
skeletal muscle
•Diaphragm and heart often have the most damage
•Binds with sodium so often see sarcoplasmic
vacuolation and resulting inflammatory changes due to
myofiber necrosis
•No tissue analyses done, must do analysis on suspected
feeds to confirm
•We often associate it with ‘cardiomyopathy’ cases in
feedlot
eed o cattle
c e - poo
poor mixingg of
o feed
eed poss
possibly?
b y?
 Petroleum industry toxicoses
•The Western Canada Beef Productivity Study in 2001-2003 showed
an association mainly with stillbirths in herds close to oil and natural
gas wells (chronic toxicity)
•With acute toxicity situations, H2S and hydrocarbons are the
principal cause of losses
•When investigating outbreaks or deaths, crucial to collect feed and
water sources for analysis
y since there are no reliable ppathologic g
lesions and tissue analyses for the numerous toxins is very expensive
and many labs cannot do these analyses
•The tissues best to collect for analysis in acute cases is liver,
liver kidney,
kidney
lung and gastrointestinal contents
•Regurgitation of hydrocarbons and H2S with aspiration pneumonia
a common cause of death in acute cases but in chronic cases there
are no reliable, consistent lesions
 Lead toxicity
y
•Less commonly seen now due to most paints being non-lead based
plus lead-free fuels now common so used oil usually does not
contain excess lead
•Old storage sites of paints, asphalt shingles, used oil and old
linoleum flooring materials still cause sporadic cases
•Kidney and liver crucial for lead analysis
•Acid fast stains on kidney from chronic poisoning cases can be used
to find lead inclusions in tubular epithelial cells
•Tips of gyri in the brain the sites of cortical damage, different than
in polio cases
•Always important to carefully search the rumen contents in suspect
cases for asphalt shingle, linoleum, paint fragments and used oil
co e s
contents
•The clinical history is critical in aiding the diagnosis
 Copper
pp toxicity
y
•Accumulated levels in the liver are suddenly released in large
amounts
•High blood copper causes lipid peroxidation, resulting in
intravascular hemolysis
•Low
Low molybdenum and low sulfate intake predisposes to
•Renal failure due to hemoglobinuria often the cause of death
• Liver enlarged and friable, spleen is dark and enlarged and
kidneys
y typically
yp y are blue-black due to hemoglobinuria
g
•Seen more often in sheep which can be poisoned by normal copper
levels in cattle rations
•Differentials for hemoglobinuria at postmortem include post-
parturient hemoglobinuria, acute severe leptospirosis and bacillary
hemoglobinuria
 Moldy
y sweet clover toxicity
y
•A common forage both as silage and hay in western Canada but less
important in recent years due to this problem
•The normal coumarin content becomes dicoumarol when mold in
sweet clover hay or silage grows
•Results in a hemorrhagic diathesis due to hypoprothrombinemia but
also lowers other clotting factors
•Fetuses in utero also involved and also seen in all ages
g of cattle
•Bleeding may be subcutaneous, intra-intestinal, perirenal, intra-
peritoneal or in any other tissue
•Easy to confirm by liver analysis for dicoumarol but also feed
analysis
•Alfalfa sometimes also contains a dicoumarol-like toxin which can
cause an identical syndrome
 Vitamin D toxicity
•Most often seen in pigs due to commercial feed mixing
errors, but occasionally seen in adult cows when
producers administer very large doses of Vit D3 as a
preventative for milk fever
•If more than two one million IU doses are given, death
with extensive tissue mineralization can occur
•The tissue most often involved are kidneys and heart
but vascular calcification can be seen in other tissues as
well
•Extensive heart and kidney involvement is usually the
cause of death
•We saw an outbreak in expensive American dogs sent
to Canada for training as hunting dogs and it was due to
commerciali l canine
i diet
di contamination
i i fromf a mill
ill
which also produced commercial pig diets
 Nitrate toxicity
• Nitrites are ten times more toxic than nitrates and
ruminal bacteria convert NO3 to NO2
• Most
M t common sources are high hi h nitrate
it t content
t t off oatt
and millet crops, especially those which have recently
been frozen
• Fertilizers and runoff into water from feedlots are other
sources of poisoning
• All tissues
i are a brown
b color
l at postmortem due d to
methemoglobin which cannot transport oxygen
• Most cases found dead but live animals clearly are
dyspneic and respond well to intravenous methylene
blue
• In our country most often
f in i fall
f ll off the
h year when
h early l
morning frosts are beginning to occur
 PHYSICAL/CHEMICAL/
TRAUMATIC CONDITIONS
 Rumenitis – Lactic acidosis
• A difficult diagnosis to make in my opinion, unless the carcass is very fresh
and a low rumen pH is present in a very fresh carcass.
• Increased fluid contents in the rumen, and dilated, congested and fluid-filled
upper small intestines
• Normally the ruminal epithelium peels off easily and this is normal within a
few hours after death. If it does not, this suggests a rumenitis with
inflammation holding the epithelium on may be present and sections should be
taken for histo examination
• Unless rumen overload is chronic, ulcers or rumen wall necrosis should not be
expected. The pH of rumen content is important but does not help a lot with
the diagnosis on feedlot rations. Length of time after death important too
• Chronic cases are much easier once mycotic infarcts and resulting areas of
hemorrhage develop ventrally in the rumen, reticulum and sometimes
omasum. Invasion of vessel walls and thrombosis by Zygomycetes group of
f
fungii are responsible
ibl for
f these
th lesions
l i
 Calfhood rumenitis
• A similar type of rumenitis occurs in neonatal calves or calves a couple of
weeks old secondary to forced-feeding of milk or other liquids administered
by esophageal feeders during treatment for diarrhea
• The esophageal feeders end up depositing the liquids in the rumen because the
reticular groove does not close and fermentation in the rumen and reticulum
then occurs
• Often antibiotics are given which can complicate the rumenitis and result in
Candida species overgrowth or ‘dysbacteriosis’
• Typically
yp y these calves respond
p to intravenous therapy
py for diarrhea problems
p
then crash and die a couple of days later due to severe rumenitis
• This is an easy diagnosis to miss if the rumen is not opened and carefully
examined and histopathology
p gy should be done as well whether it is suspected
p or
not
• Candida overgrowth sometimes occurs, but Clostridial and other bacterial
species
p are more often involved
• Necrosis is much more common histologically than appreciated grossly
 Intestinal/mesenteric volvulus
•Young calves commonly die acutely from intestinal
volvulus and extensive pathologic workup usually does
not find predisposing causes for why this happens
•Often the entire intestinal mesentery is involved or only
a long segment of especially the lower small intestine
•Need to rule out a hemorrhage enteritis such as Cl.
pperfringens
g type
yp C
•Histologically seeing extensive lamina propria
hemorrhage and marked engorgement of large veins
throughout the intestinal wall is characteristic
•Histopathologic rule-out of other primary diseases is
important
 Traumatic Reticuloperitonitis
•Commonly known as hardware disease
•In
In western Canada,
Canada wire bristles from barn brooms,
brooms fencing staples
and nails of various sources are usually responsible
•Rumen magnets are often used in higher priced dairy operations to
aid in prevention
p
•A great variety of pathologic processes seen with but include:
-acute to subacute fibrinous pericarditis
-fibrinous peritonitis, localized or generalized
-splenitis, bacterial and purulent
-liver abscesses
-vagus indigestion due to adhesions around vagus nerve
b
branches
h
-rupture of a large artery resulting in abdominal hemorrhage
-bacteremia with vegetative endocarditis and sequelae
-acute
acute renal cortical necrosis secondary to toxicity and
hypovolemic shock
 Electrocution

•Our most common cause is lightning strikes

•It is nice if streaks of burnt hair are seen but this is not
common in my experience in lightning strikes
•Circumstantial
Circumstantial evidence, clinical history and other rule
outs are very important
•I have seen multiple animals die at watering stations
where
h the th watert and/or
d/ metalt l watering
t i troughs
t h are
electrified by high voltage electrical lines often with
bare, uninsulated wires or malfunctioning electrical
devices used to prevent freezing of drinking water
•There are no consistent, useful histologic changes in
my experience
 Breeding injury peritonitis

•Large herd bulls mounting young beef heifer calves on

pasture can result in vaginal wall perforation
•The result is a severe, diffuse, fibrinous peritonitis and
death occurs fairly acutely
•Failure
Failure to properly examine the vaginal tissues can
easily result in a misdiagnosis
 Balling gun cellulitis

•Essentially this is caudal pharyngeal rupture due to

over-zealous use of ballingg gguns and results in
periesopheal cellulitis
•The Franklin Serum Company use to sell a spring-
loaded balling gun and this caused this problem not
uncommonly
•Extensive neck swelling and pockets of necrotic
material often seen to contain fragments of undissolved
medication boluses
 Thermometer injury peritonitis

•Pen-riders
id in i feedlots
f dl sometimesi ride
id through
h h the
h pens
on horseback and will take the temperatures of cattle by
simply
p y leaningg over and shovingg digital
g thermometers
into the rectum of cattle
•Occasionally this results in perforation of the wall of
the rectum and a diffuse
diffuse, severe fibrinous peritonitis and
death occurs
•Unless the terminal rectum is carefully examined, the
cause off the
h severe peritonitis
i i i can beb easilyil missed
i d
 Plant awn glossitis
•Especially
p y in dairyy cattle on silage
g rations,, embedded
barley, foxtail or bearded wheat awns become
embedded into the dorsal transverse groove (sulcus
lingualis) of the tongue not uncommonly
•These predispose to woody tongue and cause drooling,
partial anorexia and loss of milk production
•They must be removed manually and a dry towel works
well to grasp the awns and pull them out
•The tongue
g has to be ggrasped p and ppulled out
extensively to see these embedded plant structures
•Intravenous sodium iodide used to work well for me in
practice after the awns were removed
 Photosensitivity dermatitis
•This
This is skin damage by photodynamic or photoreactive
agents/pigments in the skin
•UV light is converted into thermal energy that causes
th skin
the ki damage
d
•The three types are classified according to the source of
the photoreactive pigment:
•1. Type I or primary
•2. Type II or aberrant endogenous synthesis 3.
•Type
Type III or secondary,
secondary also known as hepatogenous
•The hepatogenous form is due to phylloerythrins from
chlorophyll which cause damage when the liver has
extensive
t i chronic
h i damage
d due
d tot something
thi else
l
 Spinal cord malacia due to
dystocia

•Fetal extractors, also known as calf-pullers, exert

tremendous pressure on the spine of the fetus and
occasionally trauma-induced malacia of the spinal cord
occurs without bone fractures occurring
•At
At necropsy, hemorrhages
h h andd malacia
l i off especially
i ll the
th
lumbar cord can be obvious and extensive
•Acute vascular-induced necrosis is seen in the cord
histologically and is similar to auto-accident trauma to
spinal cords of small animals when no vertebral
fractures are found
GENETIC & CONGENITAL
CONDITIONS
 G
Growth
th arrestt li
lines in
i bones
b
•Linear to irregular
g zones of denser than normal
metaphyseal bone are commonly seen in aborted fetuses
or calves born weak and that die as neonates or in
stillbirths
•A variety of acute insults in utero can result in
temporary cessation of bone growth in utero
•We routinely look in long bones such as the femur for
these arrest lines which suggest some temporary insult
in utero
•In our experience, BVDV infection in calves is one of
the most common causes but many nutritional
deficiencies or other insults or perhaps toxicities can
also be involved
 I utero
In t growth
th retardation
t d ti

•This is when calves are born abnormally small but all

organs and tissues are of normal relative proportions to
each other
•In Canada, in utero energy deficiency is the most
common cause
•Searching
Searching for infectious causes in the tissues is always
unsuccessful
•Trace mineral analyses are also not useful in our
experience
 Dermatosparaxis
p
•In several species is often known as collagen dysplasia,
Ehlers Danlos syndrome,
y , hyperelastosis
yp cutis,, cutis laxis
or cutaneous asthenia
•We see sporadic cases in several breeds of cattle but
most of my cases have been in Simmental or Charolais
cattle
•The skin lifts up easily into folds (hyperextensibility),
b
becomes di
discolored
l d andd easily
il tears
•Sometimes joint laxity is seen along with skin lesions
•Occasionallyy this collagen
g defect pproblem is not
recognized until the animal is a few months old
•The diagnosis can be made histologically if skin from
both sites of separation and non-separation are
examined
 C
Congenital
it l spinal
i l stenosis
t i
•A
A number of herds in western Canada have experienced high
newborn calf losses due to a spinal cord stenosis and vertebral
osteopetrosis type syndrome caused by a mycotoxin of Fusarium
poae which grows on barley kernels
•Barley straw ingested by the cows during winter months results in
the condition in the fetus
•The same mycotoxin has caused similar problems in newborn
human babies in parts of Russia
•100% of the calf crop can be affected
•Clinical signs include posterior paralysis or paresis, shortened
li b varus deformity
limbs, d f it off the
th front
f t limbs,
li b brachygnathia
b h thi off the
th
upper jaw, and dome-shaped cranium
•Reference: Ribble et al. (1993) Can.Vet.J., 34, 221
 Congenital porphyria
• Also called osteohemochromatosis or congenital erythropoietic
porphyria
• In feedlots most likely to be an incidental finding at necropsy or
slaughter but some cases will manifest clinically with cutaneous
photosensitization
• Bones and teeth are brown in color and urine may have a brown
color as well
• Woods lamp examination results in red fluorescence of teeth and
bones – dramatic
• Most
M t common in i shorthorns
h th andd crosses off
• Rarely in Holstein cattle
• Does not affect performance unless severe photosensitivity results
in skin damage
 Congenital melanosis

•A variety of tissues can occasionally show melanosis at

birth and this is of no significance to the calf
•Meninges of the brain, adrenal glands, lung tissue, liver
and kidneys are common sites
•They
They simply need to recognized as nonpathologic
changes
 Intestinal segmental aplasia

•Also known as intestinal atresia

•These
These animals die of autointoxication within a few
days after birth
•The most common sites are colon and distal small
i t ti in
intestine i calves
l
•It is thought that those cases involving the colon in
calves are inherited
 Epidermolysis bullosa

•A congenital skin disease with defects at the dermal-

epidermal basement membrane zone resulting in
epidermal-dermal
id ld l separation
i
•Calves born with Nikolsky’s sign or with easily lifted
off pportions of skin
•Histologically clefts at the basement membrane zones
are seen
•We
We have seen cases in Aberdeen Angus and Romagnola
calves
•A disease of the same name occurs in Clydesdale foals
IMMUNOLOGIC DISEASES
 Allergic pneumonitis

•Reported more commonly in parts of Europe but we do

see occasionally see in dairy cattle in small high-
moisture housing situations where moulds are
extensively growing
•This
This should not be confused with atypical interstitial
pneumonia as we see it either in feedlot cattle or adult
cattle with lush pasture-associated AIP
 Post-vaccination encephalitis
p
•On rare occasion, a few days post-vaccination feedlot
cattle develop neurologic signs and die
•Histologically there is extensive mixed cellular
inflammatory changes in the medulla oblongata but
extending into the midbrain and cerebellum with acute
neuronal necrosis common
•This is thought to be a form of ‘allergic encephalitis’
where the vaccine triggers an autoimmune type reaction
in the CNS
•I have seen a couple of cases suspected of being caused
by IBR vaccines but IBR antigen in the brain by IHC
cannot be used to confirm this
•Post-vaccination
os v cc o encephalitis
e cep s in dogs iss a similar
s
condition but distemper antigens in the brain are
abundant
 Allergic dermatitis
•Milk allergy in adult dairy cows is an example but
occasionally diet origin allergies are thought to occur in
cattle as in all other species
•Histologically some superficial perivascular
eosinophils in most ruminants is normal so do not rely
on this histologic finding to make this diagnosis
•Most cases are idiopathic in that the allergen source is
not known
•A dramatically severe eosinophilic dermatitis with
extensive epidermal necrosis and/or hyperplasia are
characteristic
•I have only seen this in adult cattle
 Amyloidosis
•Most
Most often an incidental finding in adult cows in
slaughter houses
•Kidneys, spleen and adrenal glands common organs
i l d
involved
•Most often is the AL form in cattle with AA type due to
chronic inflammatory conditions less common
•Congo red stains with and without potassium
permanganate treatment can differentiate between the
two types
•Damage to the organs is strictly due to displacement or
crowding of cells
NEOPLASTIC DISEASES
 L
Lymphosarcoma
h

•Enzootic bovine leukosis is caused by a retrovirus

•Another form is known as sporadic and is not known to
be associated with the BLV
•The sporadic form can be juvenile, thymic and
cutaneous forms
•We
We do not have IHC for the BLV
•Known variably as bovine lymphosarcoma, leukemia
and malignant lymphoma
•Cases can be confined to local and often unusual sites
such as spinal meninges
 Uterine carcinoma

•These are most often diagnosed in adult cattle at

slaughter
•Unusual in that the original endometrial tumor can be
small and hard to find yet there is very widely
disseminated neoplastic tissue in other sites, such as
lung, kidneys, liver and elsewhere
•Highly scirrhous tumors, meaning associated with
ab ndant fibro
abundant fibrouss tissue
tiss e deposition
 Squamous cell carcinoma

•By far the most common site in cattle is the eye in so-
called
ll d cancer eye
•Other sites in cattle include branding sites and rarely
dehorningg sites
 Ph h
Pheochromocytoma
t

•A malignant tumor of the adrenal medulla epithelial

cells diagnosed most often in the slaughter house in
adult cattle
•Can invade the posterior vena cava as in dogs
•Are often very large at necropsy and dark yellow to
brown
•Do not cause excess epinephrine / norepinephrine
production in cattle as they sometimes do in dogs
•Can be widely disseminated if seen to invade the
posterior vena cava
 Mesothelioma

•Can be seen in all ages of cattle, including a pleural

form in newborn calves
•Usually
U ll pleural
l l or peritoneal
i l
•I saw two cases in adult cattle histologically in the
Western Canada Beef Productivityy Study y
 Schwannoma and neurofibroma

•The latter can occur in cattle cutaneous nerves similar

to a similar condition in man known as von
Recklinghausen’s disease
•I have seen a couple of adult cow Schwannomas as
small lesions on the epicardial nerves of the heart
•If they occur involving spinal nerve roots, then
progressive paralysis can occur
 Intestinal carcinoma

•Not as common in cattle as intestinal lymphosarcoma

•Rarely
Rarely seen in cattle except in old cows
•Reported to commonly be associated with Bracken fern
toxicosis (bovine enzootic hematuria) but we have not
seen this
thi in
i western
t Canada
C d to t my knowledge
k l d
 Meningioma

•The second most common nervous tissue tumor in

cattle after Schwannomas
•Can occur in the brain or spinal cord meninges
•Similar to this tumor in cats, cattle can have more than
one of these tumors, i.e., be multicentric
•Several patterns seen, based on different morphologies
and types of stroma
 Granulosa cell tumor

•The most common ovarian tumor seen in cattle

•Rarely
Rarely seen as malignant with metastasis
•Is a stromal ovarian tumor
•Single to multiple rows of round to columnar cells
li i fluid-filled
lining fl id fill d cystic
ti centers
t
•The tumor cells are often vacuolated or more like
luteinized granulosa cells
 Mast cell tumors

•Very uncommon but can be seen in cattle of all ages

and usually are cutaneous tumors
•Rarely a juvenile form is seen and can be located in
unusual sites such as the calf case being shown in the
following photos
•If undifferentiated, metachromatic stains such as
toluidine blue or Giemsa stains work well
•With the above stains,, the cytoplasmic
y p ggranules are
dark purple, the surrounding tissues blue
 Bile duct carcinoma

•Rarely seen in cattle but occur in all species.

•Are single to multiple in the liver parenchyma, are
raised, pale and often have a central depressed or
umbilicated surface
•Often are scirrhous, meaning the cords or nests of cells
induce fibrous tissue production
•Oft metastasize
•Often t t i by b lymphatic
l h ti or transcoelemic
t l i means
•Local lymph nodes often contain metastatic tumor cells
•The neoplastic cells resemble biliary epithelial cells,
but metastatic epithelial tumors from other sites need to
be considered, such as intestinal or uterine origin
 Newborn calf disseminated
neoplasms
•Occasionally we see disseminated neoplasms in
newborn calves
•Some
S are llymphosarcoma,
h bbut often
f theyh are
mesenchymal or epithelial tumors of unknown cell of
g
origin
•The following case images had extensive IHC stains
done but the cell of origin could still not be determined
 ACKNOWLEDGEMENTS

•The Department of Veterinary Pathology, University of

Saskatchewan for the opportunity to pursue such a
rewarding career
•To
To all pathologists and staff of the Dept. of Vet. Path. And
Prairie Diagnostic Services for contributing many of the
images used in this electronic atlas.
•T Drs Debbie Haines andd Eugene
•To E gene Janzen
Jan en for
f their
th i roles
l
in the development of an excellent diagnostic service, and
especially the immunohistochemistry service at the Western
College of Veterinary Medicine, Saskatoon, Saskatchewan
•The late Dr Otto Radostits for his enormous contribution
to large animal veterinary practice worldwide